Replication stress underlies many genomic alterations in cancer cells. In this issue of Developmental Cell, Benedict et al. show that WAPL-dependent cohesin removal is needed to restart DNA synthesis at stalled forks and promote survival following replication stress, uncovering an unexpected link between stress and sister chromatid cohesion loss.

中文翻译：

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衔接与连贯在是走出了停滞不前的复制叉重新启动

复制压力是癌细胞中许多基因组改变的基础。在本期《发育细胞》中，本尼迪克特等人。结果表明，必须去除WAPL依赖的黏着蛋白才能在停滞的叉子处重新开始DNA合成并提高复制压力后的存活率，从而揭示压力与姐妹染色单体内聚力损失之间的意外联系。